Evidence map›Paper›PMID 25257256›Full record

ReviewFree radical biology & medicine2015

Hypoxia and free radicals: role in tumor progression and the use of engineering-based platforms to address these relationships.

Abigail Hielscher, Sharon Gerecht

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Free radical biology & medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 101 citations in OpenAlex.

  1. Article
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  18. Green synthesis ofFrontiers in chemistry · 2023
    Article
  19. Lipid peroxidation of immune cells in cancer.Frontiers in immunology · 2023
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Abigail HielscherDepartment of Biomedical Sciences, Georgia Philadelphia College of Osteopathic Medicine, Suwanee, GA 30024, USA; Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, MD 21218, USA; Johns Hopkins Physical Sciences-Oncology Center, Johns Hopkins University, Baltimore, MD 21218, USA; Institute for NanoBioTechnology, Johns Hopkins University, Baltimore, MD 21218, USA. Electronic address: abigailhi@pcom.edu.
Sharon GerechtChemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, MD 21218, USA; Johns Hopkins Physical Sciences-Oncology Center, Johns Hopkins University, Baltimore, MD 21218, USA; Institute for NanoBioTechnology, Johns Hopkins University, Baltimore, MD 21218, USA. Electronic address: gerecht@jhu.edu.
Johns Hopkins University · US

Funding

TRANS NETWORK PROJECTSU54CA143868 · NCI · JOHNS HOPKINS UNIVERSITY · PI SEARSON, PETER C · 2009 to 2013
$13.7M
NCI NIH HHS U54 CA143868NCI NIH HHS U54CA143868
6 · The paper itself

Abstract

Hypoxia is a feature of all solid tumors, contributing to tumor progression and therapy resistance. Through stabilization of the hypoxia-inducible factor 1 alpha (HIF-1α), hypoxia activates the transcription of a number of genes that sustain tumor progression. Since the seminal discovery of HIF-1α as a hypoxia-responsive master regulator of numerous genes and transcription factors, several groups have reported a novel mechanism whereby hypoxia mediates stabilization of HIF-1α. This process occurs as a result of hypoxia-generated reactive oxygen species (ROS), which, in turn, stabilize the expression of HIF-1α. As a result, a number of genes regulating tumor growth are expressed, fueling ongoing tumor progression. In this review, we outline a role for hypoxia in generating ROS and additionally define the mechanisms contributing to ROS-induced stabilization of HIF-1α.We further explore how ROS-induced HIF-1α stabilization contributes to tumor growth, angiogenesis, metastasis, and therapy response. We discuss a future outlook, describing novel therapeutic approaches for attenuating ROS production while considering how these strategies should be carefully selected when combining with chemotherapeutic agents. As engineering-based approaches have been more frequently utilized to address biological questions, we discuss opportunities whereby engineering techniques may be employed to better understand the physical and biochemical factors controlling ROS expression. It is anticipated that an improved understanding of the mechanisms responsible for the hypoxia/ROS/HIF-1α axis in tumor progression will yield the development of better targeted therapies.

Indexed as

Disease ProgressionHumansHypoxiaNeoplasmsReactive Oxygen SpeciesReactive Oxygen SpeciesAngiogenesisHIFHypoxiaMetastasisROSTumorigenesis

Identifiers

PMID25257256
PMCPMC4339408
OpenAlexW2018948980

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.